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Mechanisms of excitotoxicity in neurologic diseases
Author(s) -
Beal M. Flint
Publication year - 1992
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.6.15.1464368
Subject(s) - excitotoxicity , nmda receptor , glutamate receptor , neuroprotection , neuroscience , receptor , metabotropic glutamate receptor , neurodegeneration , medicine , pharmacology , biology , disease
Excitotoxicity refers to neuronal cell death caused by activation of excitatory amino acid receptors. A substantial body of evidence has implicated excitotoxicity as a mechanism of cell death in both acute and chronic neurologic diseases. A major recent advance has been the successful cloning and expression of the N‐ methyl‐ d ‐aspartate (NMDA), non‐NMDA, and metabotropic glutamate receptors. The cellular mechanisms responsible for cell death after activation of these receptors are still being clarified. In acute neurologic diseases such as stroke and head trauma, excitotoxicity may be related to excessive glutamate release. In chronic neurodegenerative diseases, however, a slow excitotoxic process is more likely to occur as a consequence of either a receptor abnormality or an impairment of energy metabolism. Recent therapeutic studies have demonstrated the efficacy of non‐NMDA receptor antagonists in experimental studies of global ischemia.— Beal, M. F. Mechanisms of excitotoxicity in neurologic diseases. FASEB J. 6: 3338‐3344; 1992.